ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Inhibiting NF-κB in the developing lung disrupts angiogenesis and alveolarization.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 117 citations in OpenAlex.
- Review
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- Clinical Interventions and Inflammatory Signaling Shape the Transcriptional and Cellular Architecture of the Early Postnatal Lung.bioRxiv : the preprint server for biology · 2025Article
- Yes-associated protein induces age-dependent inflammatory signaling in the pulmonary endothelium.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Yes-associated Protein Induces Age-dependent Inflammatory Signaling in the Pulmonary Endothelium.bioRxiv : the preprint server for biology · 2025Article
- Decoding tumor angiogenesis: pathways, mechanisms, and future directions in anti-cancer strategies.Biomarker research · 2025Review
- Placental Gene Therapy for Fetal Growth Restriction and Preeclampsia: Preclinical Studies and Prospects for Clinical Application.Journal of clinical medicine · 2024Review
- CREB1 Silencing Protects Against Inflammatory Response in Rats with Deep Vein Thrombosis Through Reducing RPL9 Expression and Blocking NF-κB Signaling.Journal of cardiovascular translational research · 2024Article
- Effect and mechanism of transient receptor potential canonical channel 3 on hyperoxic lung injury in neonatal rats.Pediatric discovery · 2024Article
- Systemic juvenile idiopathic arthritis-associated lung disease: A retrospective cohort study.World journal of clinical pediatrics · 2024Article
- Prevention of Inflammatory Disorders in the Preterm Neonate: An Update with a Special Focus on Bronchopulmonary Dysplasia.Neonatology · 2024Review
- Modulation of recovery from neonatal hyperoxic lung injury by sex as a biological variable.Redox biology · 2023Article
- Endothelial-specific loss of IKKβ disrupts pulmonary endothelial angiogenesis and impairs postnatal lung growth.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Stem/Progenitor Cells and Related Therapy in Bronchopulmonary Dysplasia.International journal of molecular sciences · 2023Review
- Angiogenic signaling pathways and anti-angiogenic therapy for cancer.Signal transduction and targeted therapy · 2023Review
- Developmental diversity and unique sensitivity to injury of lung endothelial subtypes during postnatal growth.iScience · 2023Article
- Developmental trajectory of extracellular vesicle characteristics from the lungs of preterm infants.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Sex-Specific Alterations of the Lung Transcriptome at Birth in Mouse Offspring Prenatally Exposed to Vanilla-Flavored E-Cigarette Aerosols and Enhanced Susceptibility to Asthma.International journal of environmental research and public health · 2023Article
- Molecular mechanisms of cell death in bronchopulmonary dysplasia.Apoptosis : an international journal on programmed cell death · 2023Review
25 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Bronchopulmonary dysplasia (BPD), a chronic lung disease of infancy, is characterized by arrested alveolar development. Pulmonary angiogenesis, mediated by the vascular endothelial growth factor (VEGF) pathway, is essential for alveolarization. However, the transcriptional regulators mediating pulmonary angiogenesis remain unknown. We previously demonstrated that NF-κB, a transcription factor traditionally associated with inflammation, plays a unique protective role in the neonatal lung. Therefore, we hypothesized that constitutive NF-κB activity is essential for postnatal lung development. Blocking NF-κB activity in 6-day-old neonatal mice induced the alveolar simplification similar to that observed in BPD and significantly reduced pulmonary capillary density. Studies to determine the mechanism responsible for this effect identified greater constitutive NF-κB in neonatal lung and in primary pulmonary endothelial cells (PEC) compared with adult. Moreover, inhibiting constitutive NF-κB activity in the neonatal PEC with either pharmacological inhibitors or RNA interference blocked PEC survival, decreased proliferation, and impaired in vitro angiogenesis. Finally, by chromatin immunoprecipitation, NF-κB was found to be a direct regulator of the angiogenic mediator, VEGF-receptor-2, in the neonatal pulmonary vasculature. Taken together, our data identify an entirely novel role for NF-κB in promoting physiological angiogenesis and alveolarization in the developing lung. Our data suggest that disruption of NF-κB signaling may contribute to the pathogenesis of BPD and that enhancement of NF-κB may represent a viable therapeutic strategy to promote lung growth and regeneration in pulmonary diseases marked by impaired angiogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.